Ischemia-reperfusion injury: evidences for translational research

Bellanti, Francesco

doi:10.21037/atm.2016.10.52

Cited by 11 publications

(11 citation statements)

References 16 publications

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“…Introduction Transient global cerebral ischemia/reperfusion (I/R, restoration of blood flow) injury is a major consequence of cardiac arrest period and resuscitation [1]. However, short duration of cerebral ischemia (less than 10 min) can lead to neuronal death within the brain especially in the hippocampus and causes learning and memory deficits [2].…”

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confidence: 99%

Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat

Moghadam

Fereidoni

2020

PLoS ONE

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Cerebral ischemia/reperfusion (I/R) injury causes cognitive deficits, excitotoxicity, neuroinflammation, oxidative stress and brain edema. Vitamin K2 (Menaquinone 4, MK-4) as a potent antioxidant can be a good candidate to ameliorate I/R consequences. This study focused on the neuroprotective effects of MK-4 for cerebral I/R insult in rat's hippocampus. The rat model of cerebral I/R was generated by transient bilateral common carotid artery occlusion for 20 min. Rats were divided into control, I/R, I/R+DMSO (solvent (1% v/ v)) and I/R+MK-4 treated (400 mg/kg, i.p.) groups. Twenty-four hours after I/R injury induction, total brain water content, superoxide dismutase (SOD) activity, nitrate/nitrite concentration and neuronal density were evaluated. In addition to quantify the apoptosis processes, TUNEL staining, as well as expression level of Bax and Bcl2, were assessed. To evaluate astrogliosis and induced neurotoxicity by I/R GFAP and GLT-1 mRNA expression level were quantified. Furthermore, pro-inflammatory cytokines including IL-1β, IL-6 and TNF-α were measured. Seven days post I/R, behavioral analysis to quantify cognitive function, as well as Nissl staining for surviving neuronal evaluation, were conducted. The findings indicated that administration of MK-4 following I/R injury improved anxiety-like behavior, short term and spatial learning and memory impairment induced by I/R. Also, MK-4 was able to diminish the increased total brain water content, apoptotic cell density, Bax/ Bcl2 ratio and GFAP mRNA expression following I/R. In addition, the high level of nitrate/nitrite, IL-6, IL-1β and TNF-α induced by I/R was reduced after MK-4 administration. However, MK-4 promotes the level of SOD activity and GLT-1 mRNA expression in I/R rat model. The findings demonstrated that MK-4 can rescue transient global cerebral I/R consequences via its anti-inflammatory and anti-oxidative stress features. MK-4 administration ameliorates neuroinflammation, neurotoxicity and neuronal cell death processes and leads to neuroprotection. PLOS ONEPLOS ONE | https://doi.org/10.1371/journal.pone.0229769 March 9, 2020 1 / 30 OPEN ACCESS Citation: Farhadi Moghadam B, Fereidoni M (2020) Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat. PLoS ONE 15(3): e0229769. https://

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confidence: 99%

Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat

Moghadam

Fereidoni

2020

PLoS ONE

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“…The cellular and molecular mechanisms regulating the inflammatory response following myocardial ischemia and reperfusion, myocardial necrosis induces complement activation and free radical generation, triggering a cytokine cascade recruiting neutrophils in the ischemic and reperfused myocardium. 18,19 Treatment with the only efficient dose of PRP-1 (4 µg, ip) could decrease the oxidative stress processes in cardiac muscle tissues at early reperfusion period causing the reduction in the reactive oxygen species, particularly superoxide anion (O2 . -) and the MDA levels up to 40-45 %, and 20-25 % compared respectively to the rest of groups.…”

Section: Resultsmentioning

confidence: 99%

“…2,3 Mechanisms underlying IRI are complex and not well understood why there is still no effective, proven therapy against IRI. 4 We have recently reported that hypothalamic proline-rich peptide-1 (PRP-1) discovered in H. Buniatyan Institute of Biochemistry NAS RA is involved in the mechanisms of cardioprotection by the maintenance of the calcium binding properties of the cardiomyocytes membrane proteins interfering with the standard molecular mechanisms of myocardial damage caused by pancreatic necrosis and/or muscle compression injury. 5,6 At the same time there is evidence that PRP-1 could protect heart tissues on the one hand via inhibition of the phospholipase А2 and the processes of ROS generation and lipid peroxidation, on the other via stimulation the activity of catalase and the energy metabolism, exhibiting membrane-stabilizing effects.…”

Section: Introductionmentioning

confidence: 99%

Hypothalamic Proline-Rich Peptide-1 Protects Against Myocardial Ischemia-Reperfusion Injury

Gevorgyan

2017

ECB

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Hypothalamic proline-rich peptide-1 (PRP-1), a neurosecretory cytokine appeared to be involved in the multiple mechanisms of cardioprotection. Dose-dependent effects of PRP-1 (4 and 8 µg) were studied in an open-chest model of myocardial ischemia-reperfusion injury (IRI). Adult male Sprague-Dawley rats underwent 40-minute left anterior descending coronary artery occlusion, under isoflurane anesthesia followed by 2 and/or 24 h of reperfusion. Groups treated with PRP-1 were compared to control. It has been revealed that the efficient dose of PRP-1 can restore in a time-dependent manner the contractile activity of the myocardium and suppress the both inflammation and necrosis via amelioration of oxidative stress in the cardiac tissues therethrough contributing to the in vivo reduction of myocardial infarct volume and an improvement the cardiac hemodynamics and coronary circulation. New studies are needed to ascertain a beneficial effect of PRP-1 in humans and its future clinic use for the myocardial IRI treatment

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“…tissue; moreover, oxidative stress stimulates Kupffer cells and leads to hepatocellular apoptosis mediated by the expression of death receptor Fas-ligand (Koek et al, 2011). Reactive species are the most relevant cause of cellular disruption in hepatic ischemia/reperfusion (Bellanti, 2016). Oxidant injury is triggered by Kupffer cells and further amplified by polymorphonuclear leukocytes (Jaeschke and Farhood, 2002).…”

Section: Redox Biology and Oxidative Stress In Liver Diseasesmentioning

confidence: 99%

Redox Control of the Immune Response in the Hepatic Progenitor Cell Niche

Bellanti

Pannone

Tartaglia

et al. 2020

Front. Cell Dev. Biol.

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The liver commonly self-regenerates by a proliferation of mature cell types. Nevertheless, in case of severe or protracted damage, the organ renewal is mediated by the hepatic progenitor cells (HPCs), adult progenitors capable of differentiating toward the biliary and the hepatocyte lineages. This regeneration process is determined by the formation of a stereotypical niche surrounding the emerging progenitors. The organization of the HPC niche microenvironment is crucial to drive biliary or hepatocyte regeneration. Furthermore, this is the site of a complex immunological activity mediated by several immune and non-immune cells. Indeed, several cytokines produced by monocytes, macrophages and T-lymphocytes may promote the activation of HPCs in the niche. On the other side, HPCs may produce pro-inflammatory cytokines induced by liver inflammation. The inflamed liver is characterized by high generation of reactive oxygen and nitrogen species, which in turn lead to the oxidation of macromolecules and the alteration of signaling pathways. Reactive species and redox signaling are involved in both the immunological and the adult stem cell regeneration processes. It is then conceivable that redox balance may finely regulate the immune response in the HPC niche, modulating the regeneration process and the immune activity of HPCs. In this perspective article, we summarize the current knowledge on the role of reactive species in the regulation of hepatic immunity, suggesting future research directions for the study of redox signaling on the immunomodulatory properties of HPCs.

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Ischemia-reperfusion injury: evidences for translational research

Cited by 11 publications

References 16 publications

Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat

Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat

Hypothalamic Proline-Rich Peptide-1 Protects Against Myocardial Ischemia-Reperfusion Injury

Redox Control of the Immune Response in the Hepatic Progenitor Cell Niche

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